Glucose Metabolism: A Sweet Relief of Alzheimer’s Disease Claudia Duran-Aniotz, Claudio Hetz  Current Biology  Volume 26, Issue 17, Pages R806-R809 (September 2016) DOI: 10.1016/j.cub.2016.07.060 Copyright © 2016 Elsevier Ltd Terms and Conditions

Figure 1 Improving glucose uptake in the brain protects against Alzheimer’s disease (AD). (A) The neurodegenerative process of AD involves progressive neuronal dysfunction and the abnormal deposition of aggregated proteins. Low glucose uptake or reduction of glucose levels in the brain is an early event in AD, leading to cognitive dysfunction and neurodegeneration. The occurrence of chronic endoplasmic reticulum (ER) stress contributes to neuronal damage in AD possibly by activating cell death mechanisms governed by the unfolded protein response (UPR). (B) Experimental strategies to enforce glucose uptake in fly models of AD by overexpressing glucose transporter 1 (GLUT-1) delay disease progression, associated with enhancement of adaptive mechanisms mediated by the UPR, possibly due to reduced expression of BiP, a well-known negative regulator of UPR stress sensors. Since the anti-diabetic drug metformin has similar protective effects, strategies to deliver GLUT-1 into the brain of AD patients, including gene therapy using the injection of adeno-associated vectors (AAV), might improve cognitive function and reduce abnormal protein aggregation. Current Biology 2016 26, R806-R809DOI: (10.1016/j.cub.2016.07.060) Copyright © 2016 Elsevier Ltd Terms and Conditions